Adrenergic stimulation of rat resistance arteries affects Ca2+ sparks, Ca2+ waves, and Ca2+oscillations

Abstract

Confocal laser scanning microscopy and fluo 4 were used to visualize local and whole cell Ca2+ transients within individual smooth muscle cells (SMC) of intact, pressurized rat mesenteric small arteries during activation of α1-adrenoceptors. A method was developed to record the Ca2+ transients within individual SMC during the changes in arterial diameter. Three distinct types of “Ca2+signals” were influenced by adrenergic activation (agonist: phenylephrine). First, asynchronous Ca2+ transients were elicited by low levels of adrenergic stimulation. These propagated from a point of origin and then filled the cell. Second, synchronous, spatially uniform Ca2+ transients, not reported previously, occurred at higher levels of adrenergic stimulation and continued for long periods during oscillatory vasomotion. Finally, Ca2+sparks slowly decreased in frequency of occurrence during exposure to adrenergic agonists. Thus adrenergic activation causes a decrease in the frequency of Ca2+ sparks and an increase in the frequency of asynchronous wavelike Ca2+ transients, both of which should tend to decrease arterial diameter. Oscillatory vasomotion is associated with spatially uniform synchronous oscillations of cellular [Ca2+] and may have a different mechanism than the asynchronous, propagating Ca2+ transients.